title: Free radicals mediate postshock contractile impairment in cardiomyocytes.
abstract: OBJECTIVE
  Previous studies demonstrated myocardial dysfunction after electrical shock and indicated it may be related to free radicals. Whether the free radicals are generated after electrical shock has not been documented at the cellular level. This study was to investigate whether electrical shock generates intracellular free radicals inside cardiomyocytes and to evaluate whether reducing intracellular free radicals by pretreatment of ascorbic acid would reduce the contractile dysfunction after electrical shock.
  
  
  METHODS
  Randomized prospective animal study.
  
  
  METHODS
  University affiliated research laboratory.
  
  
  METHODS
  Sprague-Dawley rats.
  
  
  METHODS
  Cardiomyocytes isolated from adult male rats were divided into four groups: (1) electrical shock alone; (2) electrical shock pretreated with ascorbic acid; (3) pretreated with ascorbic acid alone; and (4) control. Ascorbic acid (0.2 mM) was administrated in the perfusate of the ascorbic acid + electrical shock and ascorbic acid groups. A 2-J electrical shock was delivered to the electrical shock and ascorbic acid + electrical shock groups.
  
  
  RESULTS
  DCFH-DA-loaded cardiomyocytes showed increased intracellular free radicals after electrical shock. The contractions and Ca2+ transients were recorded optically with fura-2 loading. Within 4 mins after electrical shock in the electrical shock group, the length shortening decreased from 8.4% +/- 2.5% to 5.6% +/- 3.4% (p = 0.000) and the Ca2+ transient decreased from 1.15 +/- 0.13 au to 1.08 +/- 0.1 au (p = 0.038). Compared with control, a significant difference in length shortening (p = 0.001) but not Ca2+ transient (p = 0.052) was noted. In the presence of ascorbic acid, electrical shock did not affect length shortening and Ca2+ transient.
  
  
  CONCLUSIONS
  Electrical shock generates free radicals inside the cardiomyocyte, and causes contractile impairment and associated decrease of Ca transient. Administering ascorbic acid may improve such damage by eliminating free radicals.
authors.affiliation: Weil Institute of Critical Care Medicine, Rancho Mirage, CA, USA.
authors.forename: Min-Shan
authors.initials: MS
authors.lastname: Tsai
authors.forename: Shijie
authors.initials: S
authors.lastname: Sun
authors.forename: Wanchun
authors.initials: W
authors.lastname: Tang
authors.forename: Giuseppe
authors.initials: G
authors.lastname: Ristagno
authors.forename: Wen-Jone
authors.initials: WJ
authors.lastname: Chen
authors.forename: Max Harry
authors.initials: MH
authors.lastname: Weil
mesh_terms: D000818:Animals; D000975:Antioxidants / Q000494:pharmacology; D001205:Ascorbic Acid / Q000494:pharmacology; D002118:Calcium / Q000502:physiology; D004554:Electric Countershock / Q000009:adverse effects; D004597:Electroshock; D005609:Free Radicals / Q000378:metabolism; D006801:Humans; D066298:In Vitro Techniques; D008297:Male; D009200:Myocardial Contraction; D032383:Myocytes, Cardiac / Q000187:drug effects / Q000378:metabolism / Q000502:physiology*; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley
chemical_list: D000975:Antioxidants; D005609:Free Radicals; D001205:Ascorbic Acid; D002118:Calcium